INTOXICAŢIA ACUTĂ GRAVĂ CU PROPAFENONĂ ABORDARE DIAGNOSTICĂ ŞI TERAPEUTICĂ
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1 10 PREZENTĂRI DE CAZ INTOXICAŢIA ACUTĂ GRAVĂ CU PROPAFENONĂ ABORDARE DIAGNOSTICĂ ŞI TERAPEUTICĂ Asist. Univ. Dr. Cristina Iolanda Vivisenco, Prof. Dr. Coriolan Emil Ulmeanu Spitalul Clinic de Urgenţă pentru Copii Grigore Alexandrescu, Bucureşti Catedra Pediatrie, Universitatea de Medicină şi Farmacie Carol Davila, Bucureşti REZUMAT Propafenona este un medicament antiaritmic ce are ca mecanism principal de acţiune blocarea canalelor de sodiu din miocard. Ingestia unei doze toxice de propafenonă determină prin intermediul efectului stabilizator de membrană un tablou clinic deosebit de grav cu răsunet cardiovascular, neurologic şi metabolic, uneori cu potenţial letal. Autorii prezintă cazul unei paciente în vârstă de 13 ani internată pentru tulburare de conducere cardiacă, convulsii şi comă, după ce a ingerat voluntar o doză toxică de propafenonă. Pacienta a fost tratată cu succes cu bicarbonat de sodiu administrat intravenos şi măsuri suportive. Autorii menţionează şi cele mai noi informaţii din literatură privind abordarea terapeutică a intoxicaţiei cu propafenonă. Cuvinte cheie: propafenonă, intoxicaţie, copil, efect stabilizator de membrană INTRODUCERE Propafenona este un medicament antiaritmic blocant al canalelor de sodiu, aparţinând clasei IC Vaughan-Williams, cu efecte slabe β-blocante şi calciu-blocante. În prezent, propafenona este utilizată îndeosebi în tratamentul tahiaritmiilor supraventriculare, atât la adult, cât şi la copil. (1) Deşi propafenona este un medicament disponibil în multe ţări, inclusiv în România, în literatură sunt raportate puţine cazuri de intoxicaţie acută la vârstă pediatrică. PREZENTARE DE CAZ O pacientă în vârstă de 13 ani a fost transferată în spitalul nostru dintr-o altă unitate medicală pentru tulburare de ritm cardiac, hipotensiune arterială, comă şi convulsii. Cu 2 ore anterior prezentării în prima unitate medicală, pacienta a ingerat în scop suicid 13 comprimate conţinând 150 mg propafenonă (doza totală 1950 mg), medicamente ce aparţineau unui membru al familiei. Pacienta era somnolentă cu scor Glasgow 11 şi următorii parametri vitali: temperatură 36,3 C, frecvenţă respiratorie 20 R/ min, saturaţie arterială în oxigen măsurată prin pulsoximetrie (SaO2) 86%, alură ventriculară 61 bpm, tensiune arterială 70/40 mmhg. Pe traseul de electrocardiogramă (EKG) se constată alternanţă de ritm sinusal şi joncţional, cu alură ventriculară cuprinsă între 55 şi 70 bpm, lărgirea complexelor QRS ( ms), bloc atrioventricular (BAV) gradul I (intervalul pr măsoară ms în perioadele de ritm sinusal) şi alungirea intervalului QT (durata intervalului QT corectat (QTc) ms) (Figura 1). S-au efectuat următoarele gesturi tera peutice: lavaj gastric, administrare de cărbune activat pe sondă nazogastrică, montarea a două linii venoase periferice, una pentru perfuzie cu ser fi ziologic şi una pentru perfuzie cu dopamină 5 μg/kgc/ min. Starea de conştienţă a pacientei s-a alterat progresiv şi a prezentat un episod de convulsii tonicoclonice generalizate care a fost cupat prin administrare de diazepam intravenos. S-a decis intubarea orotraheală şi ventilarea mecanică. S-a luat legătura telefonic cu personalul medical din secţia Toxicologie-Te rapie Intensivă a spitalului nostru, care a recomandat administrarea unui bolus de bicarbonat de sodiu în doză de 1 mmol/kgc şi transferul urgent interspita licesc. Pacienta a ajuns Adresa de corespondenţă: Asist. Univ. Dr. Iolanda Cristina Vivisenco, Spitalul Clinic de Urgenţă pentru Copii Grigore Alexandrescu, Bd. Iancu de Hunedoara nr , sector 1, Bucureşti iolanda.vivisenco@gmail.com 298 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXII, NR. 3, AN 2013
2 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXII, NR. 3, AN în Unitatea Primiri Urgenţe (UPU) a spitalului nostru la 5 ore după ingestie în stare critică, in conştientă, hipotonă, intubată orotra heal şi ven tilată mecanic, cu pupile midriatice, slab reactive, cianoză perioronazală şi a extremităţilor. Evaluarea funcţiilor vitale arăta: temperatură 36,4 C, frecvenţă respiratorie 14 R/min, SaO2 75%, alură ventriculară 74bpm, tensiune arterială 75/50 mmhg. EKG înregistrată la sosirea în UPU evidenţia ritm joncţional accelerat cu alură ventriculară 85 bpm, complex QRS larg (140 ms) şi interval QT lung (QTc 530 ms) (Figura 2). Analizele de laborator efectuate în UPU au arătat acidoză metabolică; pro bele renale, hepatice precum şi troponina I, creatin kinaza-mb şi peptidul natriuretic cerebral erau în limite normale (Tabelul 1). S-a efectuat examen to xicologic rapid al urinii, care nu a detectat barbiturice, amfetamine, cocaină, metamfetamine, ecstasy, opi a- cee, antidepresive triciclice sau marijuana. Testul a fost pozitiv pentru benzodiazepine, utilizate pen tru cuparea crizei de convulsii. Pacienta a fost internată în secţia de Terapie Intensivă unde s-a continuat administrarea de soluţii cristaloide (soluţie Ringer, ser fiziologic) şi dopamină 5 μg/kgc/min pentru corectarea hipotensiunii. S-a repetat administrarea de bicarbonat de sodiu 1 mmol/kgc în bolus. La 4 ore de la internare starea generală s-a ameliorat, coma s-a superficializat, iar parametrii hemodinamici erau în limite normale: alura ventriculară 90 bpm, tensiunea arterială 109/60 mmhg. Analizele de la borator au obiectivat dispariţia acidozei (Tabelul 1), iar traseul EKG era normal. La 6 ore de la internare pacienta era prezentă în mediu, respira spontan şi s-a decis detubarea. La 20 de ore de la internare a fost transferată în secţia Toxicologie cu stare generală ameliorată, echilibrată respirator şi cardiovascular (alură ventriculară 90 bpm, tensiune arterială 100/50 mmhg). Pacienta a fost evaluată psihologic, primind recomandarea de a urma consiliere psihiatrică în ambulator. În ziua 5, parametrii biologici, EKG şi examenul ecocardiografic erau în limite normale, pacienta fiind externată în stare bună, fără sechele. DISCUŢII Propafenona, similar celorlalţi agenţi farmacologici din clasa I Vaughan-Williams, acţionează la nivelul miocardului prin blocarea canalelor de sodiu, interferând astfel cu faza 0 a potenţialului de FIGURA 1. Ritm sinusal alternând cu ritm joncţional, BAV gradul I, complexe QRS largi şi interval QT lung
3 300 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXII, NR. 3, AN 2013 FIGURA 2. Ritm joncţional accelerat cu complexe QRS largi şi interval QT lung TABELUL 1. Analize de laborator Interval de referinţă La internare La 4 ore de la internare La 24 de la internare ph 7,35-7,45 7,17 7,50 7,43 Exces de baze (mmol/l) ,5 3,5 1,5 Bicarbonat (mmol/l) Uree (mg/dl) Creatinină (mg/dl) 0,5-1, ,6 0,6 ALT (U/L) AST(U/L) CK-MB (ng/ml) 0-4, Troponina-I (ng/ml) 0-0,4 0, BNP(pg/ml) ,9 - - Sodiu (mmol/l) Potasiu (mmol/l) 3,5-5, ,5 3.0 Clor (mmol/l) ALT alanin aminotransferaza; AST aspartat aminotransferaza; CK-MB creatinkinaza-mb (miocardică); BNP peptidul natriuretic cerebral ac ţiune. Acest mecanism este cunoscut în literatură ca efect chinidin-like, efect stabilizator de membrană sau efect anestezic local. (2) Spre deosebire de medi camentele antiaritmice din clasele IA şi IB, propafenona nu influenţează durata potenţialului de acţiune şi nici faza de repolarizare. (2,3) În plus, propafenona are şi efecte slabe β-blocante şi calciublocante. (1,4) Intoxicaţia cu propafenonă a fost raportată în literatură în cazul ingestiei unor doze de mg. Nivelul seric terapeutic este ng/ml, în timp ce nivelul seric toxic este ng/ml. (4) În cazul pacientei noastre, cunoşteam doza ingerată pe baza anamnezei, dar nu am avut posibilitatea de a doza nivelul seric de propafenonă. Ingestia unei doze toxice de propafenonă afectează funcţia de conducere intracardiacă, ceea ce se traduce prin modificările traseului EKG: lărgirea complexului QRS, aplatizarea undelor T, alungirea intervalului pr şi a intervalului QTc. Aceste modificări pot precipita aritmii ventriculare grave (tahicardie ventriculară, torsada vârfurilor, fibrilaţie ven triculară) şi preced şocul cardiogenic şi stopul cardiac. (3,4,5) Coma şi convulsiile complică tabloul clinic al intoxicaţiei cu propafenonă. Nu este complet cunoscut mecanismul prin care propafenona produce afectare neurologică. Aceasta ar putea fi explicată prin hipotensiunea arterială ce apare secundar tulburării de conducere intracardiacă, cauzând hipoperfuzie cerebrală. Hipoxia şi acidoza secundare convulsiilor pot agrava manifestările cardiotoxice. (3,4,6,7) Pacienta noastră a prezentat un unic episod de convulsii tonicoclonice generalizate ce a fost cupat prin administrare de diazepam. Rar, în tabloul clinic al intoxicaţiei cu propafenonă au fost semnalate hemoliză, agranulocitoză, ataxie, afectare hepatică şi pulmonară. (6,8) Nu am
4 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXII, NR. 3, AN observat nici unul din aceste efecte în cazul prezentat. Nu există antidot specific în intoxicaţia cu propafenonă, măsurile suportive fiind prioritare: securizarea căilor aeriene, obţinerea unei linii venoase şi monitorizarea activităţii electrice cardiace. (2) Decontaminarea gastrointestinală prin lavaj gastric şi administrare de cărbune activat va fi luată în considerare în prima oră de la ingestie, doar dacă pacientul este asimptomatic, altfel existând risc de aspiraţie. (8,9) În cazul nostru, s-a efectuat lavaj gastric şi s-a administrat cărbune activat în momentul prezentării în prima unitate medicală, la 2 ore de la ingestie. Creşterea eliminării toxicului prin măsuri de epurare extrarenală este inutilă, deoarece pro pafenona are un volum mare de distribuţie şi se leagă puternic de proteinele plasmatice. (2,3) Administrarea de bicarbonat de sodiu este indicată dacă se constată lărgirea complexului QRS pe EKG, prezenţa tulburărilor de ritm sau de conducere şi/sau a hipotensiunii arteriale. Bolusuri de 1-2 mmol/kgc vor fi administrate repetat, până când pacientul devine stabil hemodinamic, cu dispariţia aritmiei şi a convulsiilor. Valoarea ţintă a ph-ului seric este 7,50-7,55. Alcalinizarea favorizează pasajul transmembranar al sodiului, contracarând efectul stabilizator de membrană al toxicului (2,3) Pacienta noastră a necesitat administrarea a 2 bolusuri de 1 mmol/kgc bicarbonat de sodiu, ulterior constatându-se ameliorarea tabloului clinic şi normalizarea traseului EKG. Hipotensiunea arterială care nu răspunde la perfuzarea iniţială de soluţii cristaloide beneficiază de administrarea de catecolamine intravenos. Instalarea şocului cardiogenic necesită măsuri suplimentare, invazive: balon de contrapulsaţie intraaortic sau asistenţă circulatorie periferică (bypass cardiopulmonar). (2,3) În cazul nostru, hipotensiunea s-a corectat cu perfuzie cu ser fiziologic şi soluţie Ringer şi perfuzie cu dopamină. În literatură sunt raportate mai multe tentative experimentale de tratament în intoxicaţia cu pro pafenonă. Perfuzia cu emulsii lipidice a fost propusă în cazurile refractare de intoxicaţie gravă cu medicamente liposolubile cu efect stabilizator de membrană. (3) Utilizarea acestora în intoxicaţia cu propafenonă a fost deja raportată, studii suplimentare fiind necesare pentru a stabili eficacitatea emulsiilor lipidice. (10,11) Datorită efectului β-blocant al propafenonei, s-a încercat utilizarea glucagonului, cunoscut antidot al intoxicaţiei cu medicamente antagoniste ale receptorilor β-adrenergici. (12,13) Efi - cacitatea administrării unor doze mari de insulină concomitent cu o perfuzie cu glucoză a fost demonstrată pentru intoxicaţia cu agenţi β-blocanţi şi blocanţi ai canalelor de calciu. Asemănarea de structură dintre propafenonă şi aceşti agenţi poate reprezenta un argument pentru utilizarea acestei terapii în intoxicaţia cu propafenonă. (8) CONCLUZII Intoxicaţia cu propafenonă, deşi rar raportată în literatură la vârstă pediatrică, este o situaţie gravă, ameninţătoare de viaţă. Diagnosticul precoce, monitorizarea cardiacă şi măsurile suportive sunt paşi esenţiali în gestionarea acestei intoxicaţii. În lipsa unui tratament specific, administrarea de bicarbonat de sodiu şi-a demonstrat eficacitatea în ameliorarea tulburărilor de conducere şi ritm cardiac, care semnează gravitatea intoxicaţiei. Menţiune: Această lucrare este efectuată în cadrul Programului Operaţional Sectorial pentru Dezvoltarea Resurselor Umane (POSDRU) , fi nanţat din Fondul Social European şi Guvernul României prin contractul nr. POSDRU/107/1.5/S/82839.
5 302 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXII, NR. 3, AN 2013 Severe acute propafenone poisoning diagnosis and therapeutic approaches Cristina Iolanda Vivisenco, Coriolan Emil Ulmeanu Grigore Alexandrescu Emergency Children s Hospital, Bucharest Pediatrics Department, Carol Davila University of Medicine and Pharmacy, Bucharest ABSTRACT Propafenone is an antiarrhythmic drug which blocks myocardial sodium channels as the main mechanism of action. Ingestion of a toxic dose of propafenone induces through the membrane stabilizing effect a clinical presentation with cardiovascular, neurological and metabolic expression, sometimes life-threatening. The authors present the case of a 13 year old female patient admitted for cardiac conduction abnormalities, seizures and coma after intentional ingestion of a toxic dose of propafenone. The patient was successfully treated with intravenous sodium bicarbonate therapy and supportive measures. The authors mention also the latest information from the literature regarding the management of propafenone poisoning. Key words: propafenone, poisoning, child, membrane stabilizing effect INTRODUCTION Propafenone is a sodium channel-blocking antiarrhythmic drug, belonging to Vaughan-Williams class IC, with a weak β- and calcium channelblocking effect. Currently, propafenone is used mainly in the treatment of supraventricular tachyarrhythmias, in both adults and children. (1) Although propafenone is a medicine available in many countries, including Romania, few cases of acute poisoning in pediatric age group are reported in the literature. CASE PRESENTATION A 13 year old female patient was transferred to our hospital from another medical facility for dysrhythmia, hypotension, coma and seizures. 2 hours prior to her presentation in the first medical facility, the patient ingested 13 tablets containing propafenone 150 mg (total dose 1950 mg) in a suicide attempt, drugs belonging to a family member. The patient was drowsy with Glasgow coma score of 11 and the following vital parameters: temperature 36.3 C, respiratory rate 20 R/min, arterial oxygen saturation measured by pulse oximetry (SaO2) 86%, heart rate 61 bpm, blood pressure 70/40 mmhg. The electrocardiogram (ECG) showed sinus rhythm alternating with junctional rhythm and heart rate between 55 and 70 bpm, QRS complexes widening ( ms), 1 st degree atrioventricular (AV) block (PR interval measures ms in the periods of sinus rhythm) and QT interval prolongation (corrected QT interval (QTc) duration ms) (Figure 1). The following therapeutic gestures were performed: gastric lavage, administration of activated charcoal via nasogastric tube, placement of two peripheral venous lines, one for normal saline infusion and one for dopamine infusion 5 μg/kg/ min. The patient had progressive impairment of consciousness and a generalized tonic-clonic seizure that was stopped with intravenous diazepam. Endotracheal intubation and mechanical ventilation were decided. A telephone call was made to get in contact with the medical staff from the Toxicology-Intensive Care Department of our hospital, which recommended one bolus of intravenous sodium bicarbonate 1mmol/kg and urgent interhospital transfer. The patient arrived in our hospital emergency unit (EU) 5 hours after ingestion in critical condition, unconscious, hypotonic, intubated and mechanically ventilated, with mydriatic and minimally reactive pupils, perioral and limbs cyanosis. Assessment of vital functions showed: temperature 36.4 C, respiratory rate 14 R/min, SaO2 75%, heart rate 74 bpm, blood pressure 75/50 mmhg. The ECG recorded on arrival in EU highlighted accelerated junctional rhythm with heart rate 85bpm, wide QRS complex (140 ms) and long QT interval (QTc 530 ms) (Figure 2). Laboratory tests performed in EU showed metabolic acidosis; kidney and liver function tests were within normal ranges, so were troponin I, creatine kinase MB and brain natriuretic peptide (Table 1). The urine toxicology screening did not detect barbiturates, amphetamines, cocaine, methamphetamines, ecstasy, opiates, tricyclic antidepressants or marijuana. The test was positive for benzodiazepines, used to stop the seizures. The pa-
6 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXII, NR. 3, AN tient was admitted in the Intensive Care Unit where the administration of crystalloid solutions (Ringer s solution, normal saline) and dopamine 5μg/kg/ min was continued to correct hypotension. A bolus of sodium bicarbonate 1 mmol/kg was repeated. 4 hours after admission, the general condition improved, coma became superficial and hemodynamic parameters were in the normal ranges: heart rate 90bpm, blood pressure 109/60 mmhg. The laboratory tests objectified the resolution of acidosis (Table 1), and the ECG was normal. 6 hours after admission, the patient was conscious and spontaneously breathing, so she was extubated. 20 hours after admission she was transferred to the Toxicology Department in fair condition, with balanced respiratory and cardiovascular parameters (heart rate 90 bpm, blood pressure 100/50 mmhg). A psychological evaluation was performed and counseling in an outpatient psychiatric service was recommended. On day 5, the biological parameters, ECG and echocardiography were normal, the patient being discharged in good condition without sequelae. FIGURE 1. Sinus rhythm alternating with junctional rhythm, 1st degree AV block, wide QRS complexes and long QT interval FIGURE 2. Accelerated junctional rhythm with wide QRS complexes and long QT interval
7 304 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXII, NR. 3, AN 2013 TABLE 1. Laboratory tests Reference ranges At admission 4 hours after admission 24 hours after admission ph 7,35-7,45 7,17 7,50 7,43 Base excess (mmol/l) ,5 3,5 1,5 Bicarbonate (mmol/l) BUN (mg/dl) Creatinine (mg/dl) 0,5-1, ,6 0,6 ALT (U/L) AST (U/L) CK-MB (ng/ml) 0-4, Troponina-I (ng/ml) 0-0,4 0, BNP (pg/ml) ,9 - - Sodium (mmol/l) Potassium (mmol/l) 3,5-5, ,5 3.0 Chloride (mmol/l) BUN blood urea nitrogen, ALT alanine aminotransferase; AST aspartate aminotransferase; CK-MB creatine kinase MB (miocardial); BNP brain natriuretic peptide. DISCUSSION Propafenone, similar to other pharmacological agents in Vaughan-Williams class I, acts in the myocardium by blocking sodium channels, thereby interfering with the phase 0 of the action potential. This mechanism is known in the literature as quinidine-like effect, membrane stabilizing effect or local anesthetic effect. (2) Unlike antiarrhythmic drugs of class IA and IB, propafenone does not influence the action potential duration and the repolarization phase. (2,3) In addition, propafenone has also weak β- and calcium blocking effects. (1,4) Propafenone poisoning has been reported in the literature in case of ingested doses of 1,800-9,000 mg. Therapeutic serum ranges are 400-1,100 ng/ml, while toxic serum ranges are 1,100-2,000 ng/ml. (4) In our patient, we knew the dose ingested by medical history, but we couldn t determine serum concentration of propafenone. Ingestion of a toxic dose of propafenone affects the cardiac conduction function, which is expressed by changes in the ECG pattern: QRS complexes widening, T wave flattening, prolongation of the PR interval and QTc interval. These changes can precipitate severe ventricular arrhythmias (ventricular tachycardia, torsades de pointes, ventricular fibrillation) which are prior to cardiogenic shock and cardiac arrest. (3,4,5) Coma and seizures complicate the clinical presentation of propafenone poisoning. Is not well understood the mechanism by which propafenone causes neurologic injury. This could be explained by arterial hypotension occurring after cardiac conduction disturbances, causing cerebral hypoperfusion. Hypoxia and acidosis secondary to seizures may worsen cardiotoxic manifestations. (3,4,6,7) Our patient experienced a single episode of generalized tonic-clonic seizures, which has been stopped by diazepam administration. Occasionally, in the clinical presentation of propafenone poisoning have been reported hemolysis, agranulocytosis, ataxia, liver and lung injury. (6,8) We did not notice any of these effects in this case. There is no specific antidote for propafenone poisoning, supportive measures having priority: securing the airway, establishing a venous line and monitoring cardiac electrical activity. (2) Gastrointestinal decontamination by gastric lavage and administration of activated charcoal will be considered in the first hour after ingestion, only if the patient is asymptomatic, otherwise there is risk of aspiration. (8.9) In our case, the gastric lavage and the administration of activated charcoal were performed when the patient arrived in the first medical facility, 2 hours after ingestion. Enhancement of drug elimination by extrarenal epuration techniques is useless because propafenone has a large volume of distribution and strong plasma protein binding. (2,3) Administration of sodium bicarbonate is indicated if QRS complex widening is noticed on ECG, rhythm or conduction disturbances and/or hypotension occur. Boluses of 1-2 mmol/kg will be administered repeatedly until the patient is hemodynamically stable, with the disappearance of arrhythmias and seizures. Target range for serum ph is between
8 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXII, NR. 3, AN and Alkalinization induces the transmembrane passage of sodium, counteracting toxic membrane stabilizing effect. (2,3) Our patient required 2 boluses of 1 mmol/kg sodium bicarbonate, afterwards clinical improvement and normalization of ECG were noticed. Arterial hypotension unresponsive to initial infusion of crystalloid solution benefits from intravenous administration of catecholamines. In case of cardiogenic shock additional invasive measures are required: intraaortic balloon counterpulsation or peripheral circulatory support (cardiopulmonary bypass). (2.3) In our case, hypotension was corrected with normal saline and Ringer s solution infusion and dopamine infusion. In literature several attempts of experimental treatment in propafenone poisoning are reported. Intravenous fat emulsion therapy has been proposed in refractory cases of severe poisoning with liposoluble drugs with membrane stabilizing effect. (3) Their use in propafenone poisoning has already been reported, further studies are needed to establish the efficacy of fat emulsions. (10,11) Due to propafenone β-blocking effect, glucagon known antidote for β-adrenergic receptor antagonists poisoning, has been used. (12,13) Efficacy of an insulin overdose associated with glucose infusion has been demonstrated for β- and calcium channel blockers poisoning. The similarity in structure between propafenone and these agents may be an argument for using this therapy in propafenone poisoning. (8) CONCLUSION Propafenone poisoning, although rarely reported in literature in pediatric age group, is a serious and life-threatening condition. Early diagnosis, cardiac monitoring and supportive measures are essential steps in the management of this poisoning. In the absence of a specific treatment, administration of sodium bicarbonate has demonstrated effectiveness in improving cardiac rhythm and conduction disturbances, which sign the severity of the poisoning. Acknowledgement: This paper is supported by the Sectoral Operational Programme Human Resources Development (SOP HRD) , fi nanced from the European Social Fund and by the Romanian Government under the contract number POSDRU/107/1.5/S/ REFERENCES 1. Ravi Kishore AG, John Camm A. Guidelines for the Use of Propafenone in Treating Supraventricular Arrhythmias. Drugs, 1995; 50: Kolecki P. Sodium Channel-Blocking Antidysrhythmics. In Brent J, Wallace KL, Burkhart KK et al. Critical Care Toxicology Diagnosis and Management of the Critically Poisoned Patient, 1st ed. Philadelphia: Elsevier Mosby, 2005: Mégarbane B. Intoxications par les stabilisants de membrane. In Baud F, Hantson P, Thabet H. Intoxications aiguës. Paris: Springer- Verlag, 2013; Clarot F, Goullé JP, Horst M et al. Case report: fatal propafenone overdoses. Case reports and a review of the literature. J Analyt Toxicol, 2003; 27: Acar E, Duran L, Sahin Y et al. Malign Arrhytmia Development Due to Propafenone Over Dose: a Case Report. Tr J Emerg Med 2012; 12(4): Arslan ED, Solakoglu GA, Yilmaz F et al. Acute Propafenone Toxicity Discovered after Unknown Onset of Symptoms. Br J Med Med Res, 2013; 3(4): Saz EU, Ucar SK, Ulger Z et al Successful treatment of suicidal mega dose of propafenone intoxication a case report. Kardiol Pol, 2010; 68(11): Bayram B, Dedeoglu E, Hocaoglu N et al. Propafenone-induced cardiac arrest: full recovery with insulin, is it possible? Am J Emerg Med, 2013; 31(2):457.e5-457.e7 9. Koppel C, Oberdisse U, Heinemeyer G. Clinical Course and Outcome in Class IC Antiarrhythmic Overdose. J Toxicol Clin Toxicol, 1990; 28(4): Ten Tusscher BL, Beishuizen A, Girbes AR et al. Intravenous fat emulsion therapy for intentional propafenone intoxication. Clin Toxicol (Phila), 2011; 49(7): Jacob J, Heard K. Second case of the use of intravenous fat emulsion therapy for propafenone toxicity. Clin Toxicol (Phila). 2011; 49(10): Wożakowska-Kapłon B, Stępień-Walek A. Propafenone overdose: cardiac arrest and full recovery. Cardiol J, 2010; 17: Ovaska H, Ludman A, Spencer EP et al. Propafenone poisoning a case report with plasma propafenone concentrations. J Med Toxicol, 2010; 6(1):37-40
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